respiratory basics

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Respiratory Basics

Most patients having a cardiovascular emergency are inneed of supplemental oxygen and in some cases airwaymanagement. The knowledge and skills necessary toprovide respiratory support are addressed in the nextthree chapters.

This chapter provides you with the basics of respiratoryanatomy and physiology. It explores airway anatomy,the mechanics of ventilation, alveolar gas exchange andgas transport.

Respiration is an umbrella term for the total process ofdelivering oxygen to the cells and the removal ofcarbon dioxide, a by-product of aerobic metabolism.This includes ventilation (inspiration and expiration),

gas exchange and gas transport.

Effective respiratory management begins with a goodhandle on respiratory anantomy and physiology. Thesetopics are not difficult. While this chapter might seemperipheral to the core content of managing cardiacemergencies, a generous share of gems and a bettergrasp of the big picture awaits within.

Relax. Take a good cleansing breath. Now, lets get to it.

Quick Contents

Respiratory Anatomy - p. 152

Respiratory Physiology - p. 157

Ventilation - p. 158

Work of Breathing- p. 161

Gas Exchange - p. 166

Oxygen Transport - p. 171

Chapter Quiz - p. 177

Summary - p. 176

Tissue Oxygenation - p. 172

If you can walk, you can dance.If you can talk, you can sing.

Zimbabwean Proverb

8

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152 Chapter 8: Respiratory Basics

Respiratory Anatomy

The respiratory system is an intimate partner with the cardiovascular system. Together,both systems in tandem provide oxygen to tissues of the body. A sufficient oxygensupply facilitates aerobic metabolism and abundant energy production (chapter 2). Aserious lack of oxygen - and thus energy - quickly impairs the organ affected.

At rest, a healthy adult requires about 250 ml/minute of oxygen to sustain life.Fortunately, respiration normally provides an abundance of oxygen, about 1000 ml perminute at rest. This abundance of oxygen provides a significant physiologic reserve.This physiologic reserve has an important preservation / protective function for thosewho are victim to a sudden cardiac death or periods of sudden hemodynamicallyunstable tachycardias and bradycardias.

Figure 8.1 Cardiorespiratory System

The heart, the vascular network and the lungs function interdependently to ensure anadequate oxygen supply to the tissues. The venous system and the right side of the heartdelivers carbon dioxide - a biproduct of aerobic metabolism - to the lungs for speedy removal(diffuses 20 times faster than oxygen). Blood oxygenated by the lungs is pumped by the leftside of the heart via the arterial system to the tissues.

Aerobic metabolism uses oxygen to produce energy in the form of adenosinetriphosphate (ATP). When glucose is burned or oxidized, as many as 36 ATP arecreated. Water and carbon dioxide are the bi-products.Anaerobic metabolismcreates only 2 ATP in the absence of oxygen with lactic acid a toxic by-product of thisreaction.


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Respiratory Anatomy 153

In addition to ventilation and gas exchange, the respiratory system engages in severalother important tasks . The lungs moderate cardiac preload, help maintain blood acid-base balance, clear toxins, serve as an endocrine organ and act as a filter for emboli. Not

one of these tasks could be sustained, though, if the lungs failed in their primaryfunction - the gas exchange of oxygen and carbon dioxide with the blood stream. Thisprocess is facilitated by the combined actions of the upper and lower airways.

The Upper Airways

The upper airways are more than just openings to the lungs. Within the first fewcentimeters of the mouth or nose, air is cleaned, humidified and the air temperature isregulated to within a few degrees of body temperature. Key upper airway structures aredepicted in figure 8.2.

Figure 8.2 Upper Respiratory Tract

Certain structures are especially key to airway management. For example, thedisplacement of the tongue posteriorly against the soft palate and posteriororopharynx is the leading cause of airway blockage in the unconscious patient.Manipulation of the mandible with a modified jaw thrust (or head tilt-chin lift) is aneffective method to lift the tongue and open the airway.

Sphenoid Sinus

Turbinate Bones

(upper)

(middle)

(lower)

Eustacian tube

Nasopharynx

Soft palateHard palate

Mandible

Oropharynx

Epiglottis

Hyoid bone

Larynx

Thyroid cartilage

Trachea

Esophagus

Vertebra


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The vallecula, the notch between the base of the tongue and the epiglottis, is animportant target during intubation. The tip of the laryngoscope blade pulls up fromthis notch to cause the epiglottis to open (in adults). The epiglottis, a leaf- shapedcartilage that acts like a trap door covering the opening to the trachea, is anothercommon site for airway obstruction. Note that an oversized oral airway can push theepiglottis closed and obstruct the opening to the trachea.

The Trachea and The Lungs

The trachea connects the upper airways to the lungs. It is composed of a number ofcartilagous rings to provide stability and patency. Along the trachea, the cricoidcartilage is an important anatomical landmark when assisting intubation or using abag-valve-mask. The membrane between this cartilage and the thyroid cartilage is thelocation for a cricothyroidotomy.

Figure 8.3 Cricoid, Trachea and Major Bronchi

The inspiratory volume provided through the mouth can be as much as five times thevolume through the nose. For those who are receiving supplemental oxygen via nasal

prongs, note that the oxygen delivered to the patient may be substantially less if theperson is mouth breathing. A simple face mask may be a more suitable method ifhypoxia is likely.

thyroid cartilage

cricoid cartilage

trachea

tracheal cartilages

left main bronchus

upper lobe bronchus

lower lobe bronchus

carina


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The trachea terminates at the carina branching to the right and left mainstem bronchus.The right bronchus typically dips at a steeper angle than the left bronchus (see Figure8.3 on the previous page). As a result, an endotracheal tube that is inserted too deeplytends to go down the right bronchus. This can cause the ventilation of only the rightlung. Similarly, most aspiration pneumonias tend to involve the right lung.

The lungs are housed in a skeletal cage shaped by the sternum, the ribs and the spine(see figure 8.4). The sternum is composed of 3 structures: the manubrium, the sternalbody and the xiphoid process. The angle of Louis is the juncture of the manubrium and

the sternal body. This landmark is significant for monitoring central venous pressureand for locating the second costal cartilage (and the 2nd intercostal space).

Figure 8.4 Skeletal Landmarks of the Chest Cage

The cricoid cartilagerings around the trachea. Compression of the cricoid willnormally not collapse the trachea (in adults) while providing an easier visual of the

larynx. During ventilations using the bag-valve-mask(not intubated), cricoid pressurecan compress and occlude the esophagus (forcing the trachea back against theesophagus). As a result of cricoid pressure, gastric inflation and vomiting can beminimized.

The 2nd intercostal space (ICS) is a significant landmark in cardiorespiratorymanagement. For example, rapid needle decompressionof a tensionpneumothorax is performed in the 2nd ICS at the mid-clavicular line. Also, the aorticvalve is often best auscultated to the right of the sternum in the 2nd ICS, thepulmonic valve to the left of the sternum in the 2nd ICS.

ManubriumAngle of Louis

Body of

Sternum

XiphoidProcess

Thoracic

Vertebrae

Ribs

Intercostal

Spaces


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The lungs are protected by 2 layers, the outside parietal pleura and the inner visceralpleura. Surfactant produced between the pleura minimizes friction and surface tensionbetween these 2 layers allowing for unimpeded separation during expiration. The

accumulation of blood or exudate in the pleural space can negate the effects of thesurfactant, increase the work of breathing and restrict lung expansion. A tear in thepleura can lead to a tension pneumothorax.

Figure 8.5 Lung Anatomy

The lungs and the skeletal structures that encase the lungs have an important relationship. Thelungs tend to recoil on expiration inwards while the rib cage (i.e. ribs, sternum and clavicles)restricts the extent of this recoil. This creates a negative intrapleural pressure between thevisceral and parietal pleura during expiration. The diaghragms role is to draw the lungsdown and thus expand the lungs causing a fall in lung pressures. As a result, air rushes in fromthe atmosphere.

For a tension pneumothorax to occur, air is inspired into both the lungs and the pleuralspace. On expiration, this air is often trapped by a flap established by the original tearthus blocking the exit hole. With each subsequent breath, the volume between thepleural linings increases. An expanding pleural space can collapse the affected lung andexert pressure on the heart, restricting diastolic filling. A severe reduction in stroke

volume can result, leading to low cardiac output and even pulseless electrical activity.


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Figure 8.6 Tension Pneumothorax to the Right Lung

Note the effects of the an expanded pleural space (tension pneumothorax) on the heart. Thefilled pleural space can collapse the effected lung and exert high pressures to the surfaces ofthe heart. As a result, the heart becomes wrapped in a confining straight jacket, preventing itfrom opening and filling. As a result, stroke volumes decrease markedly.

Within the lungs, the respiratory tree branches from the main bronchi to the smallerbronchioles becoming narrower but exponentially more plentiful with each successivebifurcation. After about 23 divisions, the respiratory brochioles terminate at about 300million alveoli. The alveoli facilitate gas exchange between the atmosphere and the

pulmonary capillaries. The alveoli are the functional respiratory units of the lungs.

Figure 8.7 The Acinus

After about the 17th generation of branching from the trachea, alveoli begin to appear alongthe respiratory bronchioles and later as terminal structures of the alveolar ducts. The alveolarducts and the alveolar sacs (which form the acinus) are the only airways that can engage ingas exchange. All airways prior to the acini are called the conducting airways. Thisconducting zone is also referred to as the anatomical dead space.

Respiratory Bronchiole

Alveoli


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The alveoli are typically situated in clusters sharing an alveolar septum (wall). Thealveolar septa contribute significantly to maintaining the shape of the alveoli. This is animportant function in reducing breathing workload as collapsed alveoli require

considerable energy expenditures to re-open.

An alveolus consists of Type I and Type II cells. The Type I cells are larger cells thatprovide the majority of the alveolar surface, which is only one cell thick. The Type IIcells are responsible for secreting surfactant, a necessary liquid medium to reducewater tension (a tendency of water coated surfaces to attract each other) within thealveolus.

Pulmonary and Bronchial Circulation

In order for gas exchange between the atmosphere and the blood stream to occur, thealveoli must come in contact with an ample blood supply. This is accomplished by thepulmonary circulation. The entire blood volume ejected from the right ventricle entersthe pulmonary circulation. Each minute the pulmonary blood flow is virtually equal tothe cardiac output ejected by the left ventricle ( about 5 litres/minute).

The right lung pumps mixed venous blood collected from the body to the left and rightpulmonary arteries. The pulmonary arteries branch successively to form abundantsmaller arteries that culminate in about 280 billion pulmonary capillaries that envelopthe alveoli. Therefore each of the 300 million alveoli are perfused by about1000capillaries. Wow!

The pulmonary capillaries are highly distensible and collapsible because of the scarcityof vascular smooth muscle and elastic fibers that are common along the systemicarteries. Thus, pulmonary vascular resistance and pulmonary arterial pressures arequite low when compared to systemic vascular resistance and systemic arterialpressures. For example, a pulmonary artery pressure could typically be only24/8 mm Hg.

A low pulmonary vascular resistance (PVR) is the key to why the right ventricularmyocardium is about 1/3 the thickness of the left ventricle. Because of a low PVR (low

afterload), the right ventricle requires less force and less muscle mass to eject bloodinto the pulmonary circulation. Because of the relatively high systemic vascularresistance of the systemic arterial system, the left ventricle must exert a much moresubstantial contractile force to eject an adequate blood supply to the tissues. Thisrequires a larger myocardial muscle mass.


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While PVR is generally low compared to systemic vascular resistance, various factorsincrease PVR and the perfusion of the pulmonary capillaries. For example, withincreased lung volumes, the pulmonary capillaries are stretched and elongated, thus

reducing the diameter of the vessel. A narrowed vessel is much more resistive to bloodflow (resistance is inversely proportional to decreases in vessel radius to the fourthpower - R4 ). Table 8.1 provides a annotated list of factors that affect PVR.

Table 8.1 Factors That Affect Pulmonary Vascular Resistance

The lungs also requires a supply of oxygenated arterial blood to sustain the lung tissues.This is provided by bronchial arteries that branch off of either the aorta or theintercostal arteries. This is called the bronchial circulation. Normally, the bronchialcirculation accounts for about 2% of cardiac output from the left ventricle. Bronchial

blood flow increases during periods of high oxygen demand i.e. conditions such asasthma that cause high breathing workloads.

The desaturated venous return from the bronchial circulation mixes largely with theoxygenated blood returning from the lungs to the left atrium. This forms a naturalright-to-left shunt of blood that bypasses the lungs. As a result, the oxygen saturationof systemic arterial blood (obtained by pulse oximetry) is slightly less than the expected100% saturation that normally occurs at the pulmonary capillaries.

Factor Effect Rationale

gravity decreased PVR in dependentregions of the lungs

the increased vessel pressure caused bygravity in dependent lung regions opencapillaries further

lung volumes increased PVR withincreased lung volumes

increased lung volume stretches, elongatesand thus narrows the pulmonary capillaries

interstitial congestion increased PVR interstitial congestion compresses andnarrows the pulmonary capillaries

positive-pressure ventilation increased PVR positive-pressure ventilation compressesand narrows the pulmonary capillaries

histamine increased PVR pulmonary vasoconstrictor

alveolar hypoxia increased PVR pulmonary vasoconstriction occurs in aneffort to redirect blood to more functional

alveoli

alveolar hypercapnia increased PVR pulmonary vasoconstriction occurs in aneffort to redirect blood to more functionalalveoli


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Flash Quiz 8.1

1. Obstruction of the upper airways is most often caused by:

a) cut up hotdogsb) the tonguec) the epiglottisd) hard candy

2. Cool air that enters the nose and mouth is warmed to within a few degrees of corebody temperature by the time it enters the lungs.

True or False

3. Each alveolus is enveloped in about (1, 10, 100, 1000) pulmonary capillaries.

4. Compression of the cricoid cartilage can be useful during:

a) intubationb) forceful vomitingc) positive pressure ventilations using a bag-valve-maskd) a and c

5. Surfactant :

a) is produced by Type I cells in an alveolusb) is a substance that reduces surface tension within an alveolusc) production increases the work of breathingd) all of the above

6. Gas exchange occurs at the (circle all that are correct):

a) alveolar ductsb) conducting airwaysc) alveoli

d) acini

7. Anatomical dead space (circle all that are correct):

a) is the space between the visceral and parietal pleurab) does not engage in gas exchangec) is reduced with an asthma attackd) is a term that refers to the conducting airways

Answers: 1.b) 2.true 3.1000 4.d) Note that cricoid pressure during forceful vomiting can result in an esophagealrupture 5.b) 6.a), c), d) 7.b), c), d)


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Respiratory Physiology 161

8. Blood flow to the lungs (circle all that are correct):

a) includes both the pulmonary circulation and bronchial circulation

b) is greater than the cardiac output from the left ventriclec) is greater than the blood flow to any other organ in the bodyd) exits through the pulmonary veins

9. The left ventricle has a larger muscle mass than the right ventricle because the leftventricle must pump blood further into the body.

True or False

10. Pulmonary vascular resistance is usually equal to systemic vascular resistance.

True or False

Respiratory Physiology

Knowing about the structures of the upper and lower airways is important to be able todifferentiate between normal and pathological findings. Understanding why and howthese structures function together to facilitate respiration is at least as important.

In general, answering the how and why things work demands attention to the finerdetails of a process. The next few sections begin with a look at the mechanics ofspontaneous and assisted breathing. We will then delve into the microscopic processesthat connect breathing with energy production: gas exchange and gas transport.

Mechanics of Ventilation

Ventilation involves inspiration and expiration, moving air into and out of the lungs.Most of us simply call it breathing. An average adult breathes in about 500-700 ml of airwith each breath at a rate of about 15 breaths a minute for a daily volume of about13,000 litres. How does air move into and out of our lungs? What factors influence theefficiency and effectiveness of breathing? This section addresses these questions.

Air moves from an area of high pressure to an area of lower pressure. As the diaphragmcontracts and pulls down, the lungs are also drawn down (inspiration). Theintrapleural pressure generated between the visceral and parietal pleural layers

Answers: 8.a), b), d) The lungs receive about 2% more blood than the cardiac output from the left ventricle due to thecontributions from both the right ventricle and the bronchial arteries. The heart receives about 10 litres of blood each minute- 5 litres to the right and 5 litres to the left. 9.d) Note that cricoid pressure during forceful vomiting can result in anesophageal rupture 10.True


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becomes increasingly negative. The visceral pleural layer connects with the lung wallwhile the parietal pleural layer connects with the chest wall (i.e. ribs). A more negativeintrapleural pressure pulls upon and opens the alveoli further.

In a closed system pressure decreases as volume increases. The expanded alveolarvolume from inspiration causes a reciprocal fall in alveolar pressure below atmosphericpressure, and air rushes into the lungs to equalize this pressure gradient.

In a closed system, pressure is inversely related to volume.

This negative-pressure ventilation, better known as breathing spontaneously, is themechanism behind normal breathing. The external intercostals and scalene musclesare also used in normal inspiration. The sternocleidomastoid muscle is an accessorybreathing muscles used during periods of rapid breathing and dyspnea.

Expiration is usually a passive process requiring minimal work during normalbreathing. As inspiratory muscles relax, the inward elastic recoil ( see page 167) of thealveolar wall reduces alveolar volume. Alveolar pressure begins to surpass atmosphericpressures and air exits the lungs. Forced expiration, as might occur with increasedbreathing rates, actively engages the abdominal and intercostal muscles to reduce thesize of the chest cavity more rapidly than the time taken at rest.

To review, spontaneous inspiration causes the pleural cavity to increase, intrapleuralpressures to become negative, and air to move from an area of higher pressure (theatmosphere) to an area of lower pressure (the lungs). During expiration the intrapleuralpressures are increased in relation to atmospheric pressure as the closed thoracic cavitydecreases in size. This causes air to flow back out to the atmosphere.

The diaphragm is the main muscle responsible for inspiration. It is innervated by thephrenic nerve, arising from the 3rd-5th cervical segments of the spine. The

accessory breathing muscles (i.e. intercostals) are innervated by nerves that arise lowin the thoracic and lumbar segments. These simple facts help explain why spinal cordinjuries in the lower back generally do not adversely affect ones breathing (thediaphragm remains functional); whereas, high cervical spinal injuries typically resultin the inability to breathe.
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For patients who require assistance breathing, a ventilator or bag valve mask (BVM)delivers air forcefully into the lungs. The air pressure created by the action of thesedevices is higher than the air pressure in the lungs. This type of ventilation is calledpositive-pressure ventilation (PPV) and it has many benefits in cardiovascularemergencies. For example, PPV can help expand collapsed alveoli or cause fluids to be

forced out of the lungs and into the blood stream i.e. to treat pulmonary edema.

What Drives Breathing?

Spontaneous breathing is unique in that it can be both a conscious and an unconsciousprocess. We can consciously speed, slow or stop breathing at will. Most often, though,breathing is an unconscious activity with rate and depth closely monitored by a host ofsensors throughout the body. With varying energy demands and stimuli, the volume ofair breathed over a minute (minute ventilation) fluctuates in kind.

Voluntary control of breathing is accomplished by the cerebrum while the involuntaryor automatic control of breathing is provided by the brain stem. A host ofchemoreceptors stimulate the brain stem to innervate the muscles responsible for

ventilation i.e. diaphragm. These receptors influence the rate and duration of breaths(see Figure 8.8).

The drive to breathe is normally stimulated by falls in the blood pH (more acidotic)most often attributed to increased carbon dioxide levels (see the section on acid-basebalance in chapter 9). Chemoreceptors in the brainstem react to hypercapnic (highCO2) blood levels with increases in breathing rates to blow off excess CO2. As a result,blood acid levels return to a target zone.

The hypercapnic drive to breathe is quite powerful. For example, minute ventilationvolumes usually increases by 2-3 litres/minute for every 1 mm Hg increment in CO2levels in an attempt to normalize blood pH. Therefore, CO2 levels of 45 mm Hg (40mm Hg is an accepted mean) can cause the minute ventilation to increase by up to 15litres/minute, almost quadrupling minute ventilation volumes.

Positive pressure ventilationdoes have its disadvantages. Positive pressureventilation can rupture the lung causing a tension pneumothorax. Positive pressure

ventilation with positive end expiratory pressure (PEEP) can increase the internalpressures on the pulmonary vasculature and reduce the venous return (preload) tothe left side of the heart. A reduction of preload may benefit those in left ventricularfailure or compromise those who are critically dependent on preload (i.e. acute rightventricular infarction).


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Figure 8.8 Regulation of Ventilation

Low blood oxygen levels can also drive breathing. Chemoreceptors in the carotidbodies respond to hypoxemia, sensing falls in blood oxygen levels (PaO2) with thestimulation of the breathing centers in the mid-brain. They react most strongly to fallsin PaO2less than 60 mm Hg, corresponding to oxygen saturations below 90% (normalPaO2is 80-100 mm Hg at sea level).

The drive to breathe is also affected by stretch receptors (associated with the vagusnerve) in the smooth muscle and mucosa of the airways that respond to increases inlung volumes. As a result of the stimulation of these receptors, respiratory ratedecreases. This is known as the Hering-Breuer reflex.

Brain Stem

(involuntary control)

Cerebrum

(voluntary control)

Effect Changes

Carotids

Vagal Effectors from

Central Chemoreceptors

(hypoxic drive)

(hypercapnic drive)

Respiratory

Centers

Lungs and Airwaysin Rate, Duration

Because the hypercapnic chemoreceptors in the brain stem usually respond first,ventilations are generally driven by hypercapic chemoreceptors. Oxygen levelsgenerally never fall below 60 mm Hg. As a result, the hypoxic drive is seldom calledupon to stimulate breathing. For those with advanced lung disease, though, the abilityto lower CO2levels decrease. Chronically high CO2levels may desensitize thehypercapnic chemoreceptors, with the hypoxia chemoreceptors called upon tostimulate breathing. For these people, the administration of high flow rates of oxygencan increase their PaO2to a level where the hypoxic drive falters. With both hypoxicand hypercapnic drives now inactive, respiratory failure is quite possible. For thosewith advanced lung disease and chronically high CO2levels, the goal isoften to improve their hypoxia without relieving it completely.This might beachieved by delivering a sufficient supply of oxygen to maintain oxygen saturationsnear 90-92%.


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Some aspects of the regulation of ventilation remain a mystery. For example, minuteventilation volumes can expand to over twenty times normal during exercise eventhough arterial pH, PaO2, and CO2would largely remain unchanged with only

marginal increases in breathing rates. Physiologists point to possible respiratoryreceptors in muscles, joints, tendons and the diaphragm as possible triggers.

Factors That Influence The Work of Breathing

Ventilations are most efficient when optimal gas exchange is achieved with a minimalbreathing workload. Disorders of the respiratory system can impair gas exchange andincrease the work of breathing. Several factors affect the efficiency and the effectivenessof breathing whether breaths are self-delivered (negative pressure) or delivered by abreathing device (positive pressure). These factors include:

inspired volume- the amount of air breathed during inspiration

airway resistance to air flow

tissue resistance- frictional resistance of lung tissues and chest wall

elastic recoil- the ability of the airways to maintain their baselineshape rather than collapse on exhalation

compliance - the distensibility of the lungs to accommodate adequatevolumes of air

breathing rate- increased minute ventilation volumes are achievedover time with an increased breathing rate

The work of breathing is a product of the work necessary to cause changes in lungvolume and pressure. For each breath, it is the pressure changes within the lungs thatcause increased lung volumes (inspiration). The primary work for each breath, then, isthe work done to produce a pressure change between the lungs and the atmosphere.

In order to cause a pressure change in the lungs, effort (work) is necessary to overcomeairway resistance, tissue resistance and elastic recoil. The work of breathing, then, isprimarily the work necesary to overcome airway resistance, tissue resistance and elasticrecoil. The work of several breaths is cumulative. As a general rule, then, the greater thelung volumes and the faster the breathing rate, the work of breathing increases.

While the work of quiet breathing consumes only about 5% of the bodys oxygencontent, difficult and rapid breathing can cost as much as 25-30% of the bodys oxygencontent. For a healthy adult during exercise, for example, an abundant physiologicalreserve satisfies this extra need (see page 152). For the cardiac patient with a lowcardiac output and pneumonia, this is likely critical.

The Resistive Work of Breathing


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The resistive work of breathing - overcoming tissue resistance and airway resistance -adds significantly to breathing workload. Normally, airway resistance accounts for themajority of the resistive work of breathing. Tissue resistance only accounts for about

20% of the total resistance of breathing. Tissue resistance occurs due to the frictionproduced between lung tissues during lung inflation. Airway resistance is the frictionbetween inspired air and the airway walls.

Three types of air flow occur, determined generally by the size of the airways. Air flowsthrough the larger airways in a turbulent fashion while air flow through the narrowbronchioles is more laminar (where air in the center of the airway moves faster than theair at the walls). As airways branch off, transitional air flow results from a mix oflaminar and turbulent air flow. The factors that determine the degree of airwayresistance change with the type of air flow.

Figure 8.9 Turbulent and Laminar Air Flow

With turbulent air flow, airway resistance is proportional to inspired air density and airvelocity. For example, denser air at sea level inspired at greater velocities (i.e. fast breathingrate) increases airway resistance in the larger airways where turbulent air flow occurs.Laminar airflow occurs in the smaller airways. Here airway resistance is a function of theairway length and the inverse of the airway radius to the fourth power. Airway resistance insmaller airways would then increase 16 times for a radius that is reduced by half. Conversely,an airway with a radius that doubles in size would have 16 times less (24) airway resistance.

Airway resistance is significant in the upper airways. When breathing through thenose, the upper airways (nasopharynx, oropharynx and larynx) account for about40% of the total airway resistance. When mouth breathing, the upper airwayresistance is about 25% of the total airway resistance. For those who are experiencingan extended and difficult wean from mechanical ventilation (i.e. a ventilator), acommon practice is the creation of a tracheostomy. Note that a tracheostomybypasses the upper airways making breathing easier.

Turbulent Air Flow

Laminar Air Flow

(air density, velocity)

(1/radius4)

Transitional Air Flow

(turbulent + laminar)


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Turbulent air flow resistance is more pronounced when the inspired air is more denseand moves with greater velocity. Turbulent air flow is noisy, providing the breathsounds audible with a stethoscope. Laminar airway resistance increases dramatically as

the airway lumen narrows. Laminar airway resistance is calculated by Poiseuilles law:

Airway Resistance = (8 x viscosity x length) / x radius4

The important point to take from this formula is that a reduced airway lumen has adramatic affect on airway resistance (increases it to the 4th power). For example, if asmaller airway is narrowed by half its original radius by such events as infection,inflammation, or bronchospasm, the airway would be 16 times ((1/0.5)4) moreresistant to air flow.

Figure 8.10 Emphysema

With emphysema, the smaller airways and the alveoli tend to collapse during forcedexpiration due to diminished elastic recoil. The work to re-expand these airways can betremendous.

Medium-sized bronchi are the prime contributors to airway resistance.Parasympathetic stimulation, increased mucous production (infection, asthma),foreign body obstruction and inflammation can narrow the bronchi, increase airwayresistance and increase the work of breathing. Conversely, sympathetic stimulationtends to dilate the bronchi. Localized hypoxia and hypercapnia dilates the smallerairways in an effort to increase ventilation, increase PO2and reduce CO2.

The Elastic Work of Breathing

Collapsed

Airway

Increased Airway

Resistance

Elastic Recoil

4(by radius )

(due to forced

expiration)


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Since lung volume is directly related to pressure change (i.e. the difference betweenatmospheric and alveolar pressures drive volume changes), the work required for eachbreath is primarily the resistive and elastic work necessary to produce a pressure

change. Besides air and tissue resistance, factors such as the elastic recoil of the lungsand the surface tension of the alveoli must also be overcome.

Figure 8.11 Elastic Recoil of the Lung and the Chest Wall

The elastic recoil of the lungs refers to the tendency of the alveoli and other lungstructures to return to their original size. As elastic recoil increases, so does the work ofbreathing. Factors that contribute to elastic recoil include alveolar surface tension (see

page 170) as well as elastin and collagen in lung tissue. Alveolar surface tensionaccounts for about 2/3 of the total elastic recoil of the lungs.

The inverse of elastic recoil is lung compliance. Lung compliance refers to the ease bywhich the lungs can increase in volume. A more compliant lung distends with less workof breathing. Technically, lung compliance is the slope between two points on apressure-volume curve. The steeper the slope, the greater the lung volume changes perunit pressure change. This is a useful concept when trying to understand how eithercompliance or elastic recoil affects the work of breathing (see Figure 8.10).

Elastic Recoil Inwards(lung structures, alveolar surface tension)

Elastic Recoil

Outwards(chest wall)

Elastic Recoil

Outwards(chest wall)


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Figure 8.12 Lung Compliance and Lung Disease

The steeper the slopes of the pressure-volume curves, the more compliant the lungs.Transpulmonary pressure is the difference between the air pressures in the trachea and thealveoli. When alveolar pressure falls below the tracheal pressure, air enters the lungs. Withlung diseases that cause interstitial congestion in the lungs and fibrosis (i.e. ARDS), elasticrecoil of the lung tissues increases, lung compliance decreases and the elastic work ofbreathing becomes more arduous.

As lung compliance increases, the elastic work of breathing is reduced. For many lungdiseases, particularly restrictive lung disease such as pulmonary fibrosis, compliancedecreases and breathing becomes more arduous. Other conditions that decrease lungcompliance include acute respiratory distress syndrome (ARDS), pulmonary edema,and pneumonia. Note that each of these diseases produce an increase in elastic recoil.and the elasic work of breathing.

Transpulmonary Pressure

Normal Lung

Atelectasis, ARDS

Normally, the highly compliant lungs expand easily. As a result, the work of breathing atrest uses only about 2% of the bodys oxygen consumption. For a healthy person, rapid

breathing does not increase the work of breathing significantly. For those with obstructive

or restrictive lung disease, though, the work of breathing at rest and with exertion cantax the muscles involved. Respiratory muscle fatigue and failure are more likely to occur

for those with lung disease.


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Elastic recoil does more than just add to the breathing workload. Elastic recoil takes thework out of expiration and maintains airway patency during sudden periods ofchanging pressures. While the larger airways contain cartilagous rings to maintain

patency, the smaller airways depend on a matrix of elastin and connective tissue toremain open.

Surfactant

The main contributor to the inward elastic recoil of the lungs is the surface tensionwithin the alveoli. Water is generally more attracted to other water molecules than it isto air (this attraction is what keeps a water droplet together). Along the inside surfaceof an alveolus, this attraction of water for itself creates a surface tension,drawing thewalls of the alveolus towards each other.

Surfactant is a chemical produced by the type II cells within the alveoli that effectivelyreduces surface tension within the alveoli. The presence of adequate amounts ofsurfactant, then, is necessary to minimize both the work of breathing and the fluidwithin the alveoli.

During periods of hypoxia and hypoxemia, the production of surfactant is curtailed.Possible complications of this lower surfactant production are increased surfacetension, collapsed alveoli (atelectasis) and fluid accumulation in the alveoli. Pulmonaryedema is but one disease that can cause low surfactant production.

Being aware of the factors that affect the workload of breathing influence respiratorymanagement. For example, a hypoxemic episode during an asthma attack oftenresponds well to agents that open the airway lumens, reduce airway resistance, decreasethe work of breathing and increase air flow to the alveoli. Supplemental oxygen may

help increase oxygen supply to the tissues. A reduction in hypoxia can also help ensureadequate surfactant production.

Its time to review the mechanics of breathing and the factors that affect the work ofbreathing with a brief quiz before we move on to the intricacies of gas exchange and gastransport.

If the work of breathing is significant, respiratory fatigue can lead to precipitous dropsin both breathing rates and inspired volumes - both signs of respiratory failure. Notethat signs of respiratory failure such as an altered level of consciousness, paradoxicalbreathing and elevated CO2levels may coincide with an apparently normal breathingrate and oxygen saturation. Being aware of the factors that influence breathingworkload is useful for predicting and treating respiratory fatigue


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Flash Quiz 8.2

1. The muscles involved in normal inspiration usually include (circle all that apply):

a) sternocleidomastoidb) internal intercostalsc) external intercostalsd) abdominale) diaphragm

2. Compliance is the inverse of elastic recoil.

True or False

3. Which of the following conditions result in an increased breathing workload (circleall that apply):

a) decreased lung complianceb) decreased elastic recoilc) narrowed airwaysd) pleural effusione) kyphoscoliosis (curvature and rotation of spine)f) restrictive lung diseaseg) obstructive lung disease

h) obesityi) rapid breathing rates

4. The alveoli open during inspiration due to the muscle tissue that surrounds eachalveoli.

True or False

5. The main muscle used for breathing is the (diaphragm, sternocleidomastoid) whichis innervated by the (vagal verve, phrenic nerve) which leaves the spine at the level ofthe level of the (lumbar vertebrae, #3-5 cervical vertebrae, 6-9 thoracic vertebrae).

6. Which of the following statements about the mechanics of breathing is false?

a) inspiration is an active processb) exhalation is a passive process at rest and during physical exertionc) accessory breathing muscles are used to increase inspiratory volumesd) negative pressure ventilations are spontaneously performed at rest

Answers: 1.c), e) 2.True 3.all but b) 4.False 5.diaphragm, phrenic nerve, #3-5 cervical vertebrae 6.b)


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7. In a closed system, as volume increases, pressure increases.

True or False

8. The chemoreceptors that stimulate breathing as a response to hypoxia are located:

a) along the inner surface of the airways in the lungsb) centrally near the respiratory center in the midbrainc) in the carotid bodiesd) all of the above

9. For those without advanced lung disease, breathing is driven primarily bychemoreceptors that monitor blood acidity (and carbon dioxide levels).

True or False

10. Respiration is accomplished with the physiological goal to provide a sufficient lungvolume with minimal breathing workload. As (compliance, air resistance) increases, sodoes breathing workload. In conditions such as emphysema, an (increased, decreased)elastic recoil can result in collapsed airways, particularly during (inspiration,expiration).

Gas Exchange and Transport

Gas exchange is vital for aerobic metabolism and energy production. Without oxygen,energy production is terribly less effective. No energy - no life. Effective oxygenationoccurs if three mechanisms occur: 1) oxygenation of the blood at the alveoli; 2) thetransport of oxygen to the tissues; and 3) the release of oxygen at the cellular level. Abreakdown in any these tasks can result in hypoxia, a lack of oxygen at the cellular level(where it really counts).

A term used perhaps as often as hypoxia is ischemia. Ischemia is a lack of oxygen to thetissues due to inadequate flow of blood (oxygen transport system). The end result,though, is similar to hypoxia - a lack of oxygen (and therefore energy) at the cellularlevel. Both hypoxia and ischemia can quickly cause cellular damage and, soon after,

cellular death. Hypoxemia is a low arterial partial pressure of oxygen (i.e. low PO2athigh altitudes is one example). Hypoxemia can cause hypoxia.

While discussions of respiratory physiology may tend to be biased towards the role ofoxygen, the transport and exchange of carbon dioxide are also important factors.Carbon dioxide levels affect oxygen transport, oxygen affinity and acid-base balance.Through O2and CO2 transport and exchange, respiration strives to maintainhomeostasis and drive energy production.

Answers: 7.True 8.c) 9.True 10.air resistance, decreased, expiration


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The structures and the mechanics of the respiratory system, as just outlined, are finetuned to minimize the workload of breathing while maximizing gas exchange. Delvingdeeper into respiratory physiology reveals many more evolutionary wonders. The

rationale behind many clinical respiratory and cardiac interventions rests in theintricacies of gas exchange and transport.

Alveolar Gas Exchange

Lets begin at the top. Air enters the trachea rapidly during inspiration. As the air passesthe bronchi on to the bronchioles about 23 successive divisions exponentially increasethe overall cross-section that the air occupies. As a result, air speed begins to slow as theair reaches the deeper bronchioles. At the alveoli, air velocity approaches zero. Here, gasmoves primarily due to diffusion alone.

Figure 8.13 The Alveoli and Oxygen Exchange

A respiratory bronchiole, the alveolar duct and the alveoli form the terminal respiratoryunit of the lungs. It is here that gas exchange occurs. About 80% of the surface area ofthe alveoli is in contact with pulmonary capillaries. The remaining 20% is commonlycalled physiologic dead space (PDS). Along areas not perfused by capillaries, gasexchange cannot occur.

The ventilation/perfusion ratio (V/Q) reflects the adequacy of inhaled volume (V) asmeasured against the amount of blood perfused (Q). Since we breathe about 4 litres ofair at rest (after anatomical dead space is subtracted) and circulate about 5 litres of

Oxygen and CO2Exchange

The total surface of the 300 million alveoli is an impressive 80 m2- about 40 times thesurface area of the skin. The lungs have significantly more contact with the atmosphere

than does the skin (or any other organ for that matter). As a result, the alveoli provide

ample surface area for gas exchange.


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blood/minute, a normal V/Q ratio then would be about 4/5 or 0.8 or 80%. Asventilation increases and lung perfusion decreases (i.e. shock states or pulmonaryembolus), the V/Q ratio increases.

Figure 8.14 Gas Exchange at the Alveolus

The capillaries carry blood that is low in oxygen (PaO2=40 mm Hg) and high in carbondioxide (PaCO2=45 mm Hg). With a higher partial pressure for oxygen (104 mm Hg) in the

alveoli, oxygen tends to diffuse into the capillaries and the red blood cells. Carbon dioxidediffuses into the alveoli. Red blood cells must squeeze through the capillaries. This providesample surface area for the oxygen to diffuse through and bond to Hgb for transport.

Gas exchange at the alveoli occurs due to diffusion alone. Only a 2 cell thicknessseparates the air within the alveoli from the blood in the capillaries. The red blood cells,the primary transport units of both oxygen and carbon dioxide, must squeeze throughthe tiny capillaries. The resulting close proximity of the red blood cell wall to thealveolus helps to facilitate rapid gas exchange.

Alveolus

Red

Blood Cell

Capillaries

PAo2 = 104 mm Hg

PAco2 = 40 mm Hg

Pao2= 40

Paco2= 45

Low ventilation with normal or high perfusion yields a low V/Q ratio. For diseaseprocesses such as pneumonia and tension pneumothorax, collapsed airways arenot ventilated, perfusion is maintained and gas exchange is hampered. As a result,some blood shunts to the left atrium without the benefit of gas exchange. If theshunt becomes significant (i.e. large part of the lung is affected), arterial oxygensaturation falls.


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With only a 2 cell separation between the inside of the alveoli and the blood, it is notsurprising that increased pressure within the capillaries (hydrostatic pressure due toback up of blood volume into the lungs i.e. left ventricular failure) can lead to fluid

accumulation in the lungs.

Gases such as oxygen and carbon dioxide freely cross between the blood and thealveoli. Gas diffusion is dependant on a difference in partial pressures of gases betweenthe alveoli and the pulmonary capillaries. Gases quickly diffuse from high pressurezones to low pressure zones. As a result, oxygen enters into the capillaries and carbondioxide exits through the alveoli.

Figure 8.15 Normal Arterial and Venous Oxygen Values

The pulmonary arterial system brings blood to the lungs that is oxygen-depleted and carbondioxide rich. After gas exchange occurs at the lungs, the pulmonary venous system delivers

oxygenated blood to the left atrium.

Diseases such as asthma and emphysema restrict the flow of air into and out of thelungs, impairing gas exchange at the alveoli. Pneumonia causes gas exchangeimpairment along regions of the pulmonary capillary bed leading to shunting, elevatedblood CO2levels and falling blood oxygen levels.

Arterial System Venous System

PO2= 80-100 mm Hg

O2sats = 95%+

PO2= 40 mm Hg

O2Sats = 75%

LU

N

G

S

Pulmonary Pulmonary

Daltons law of partial pressure states that the total pressure of a volume of gasequals the sum of the partial pressures of each gas that constitute the gas mixture.At sea level, the pressure of air (atmospheric pressure) is 760 mm Hg. Sinceroughly 21% of air is oxygen, the partial pressure of oxygen is equal to 21% of 760mm Hg (answer is 158 mm Hg). If a person is breathing 50% oxygen via a facemask, then the partial pressure of oxygen inspired is equal to 50% of 760 mm Hg(answer is 360 mm Hg).


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Normally this gas exchange (diffusion) occurs in 1/4 second. Because the red blood cellgenerally takes about 3/4 of a second to flow (or squeeze) by the alveoli, the red bloodcell has more than sufficient time to complete the gas exchange. In high output states

(i.e. extreme exercise), the increased speed of blood flow can reduce the opportunityfor gas exchange if red blood cells are across the alveolar membrane for a period lessthan 1/4 second.

Figure 8.16 The Red Blood Cell and the Pulmonary Capillaries

The red blood cell (about 8 microns in diameter) must re-shape and squeeze through thenarrow capillaries (about 6 microns in diameter). Gas exchange occurs in just 1/4 second.The red blood cell (RBC) is proximate to alveoli for approximately 3/4 second during normalconditions. During periods of high cardiac output (i.e. extreme exercise), gas exchange maybe incomplete as the faster moving RBC may be proximate to alveoli for less than 1/4 second.

Other causes of failure to oxygenate the blood include airway obstruction, respiratoryfailure, carbon monoxide poisoning and low oxygen gradients (i.e. high altitude).Respiratory failure is usually diagnosed with the partial pressure of oxygen in thearterial system (Pao2) falling below 50 mm Hg or the partial pressure of carbon dioxide(Paco2) being over 50 mm of Hg.

As mentioned, respiratory failure is usually associated with both low oxygen levels andhigh CO2levels. The high CO2levels are associated with increased carbonic acid in theblood. The lower blood pH levels associated with high CO2 concentrations is called

Red Blood Cell

Capillary Wall Time Proximal to Alveolus: 3/4 seconds

Time for Gas Exchange: 1/4 seconds

PulmonaryCapillary

While most instances of poor oxygenation produces cyanosis, carbon monoxide (CO)poisoningis the exception. Hemoglobins affinity for carbon monoxide is about 240times that of oxygen. Carbon monoxide quickly binds to hemoglobin at the sites usually

reserved for oxygen. This causes the hemoglobin to reflect a bright red hue typical of

full oxygen saturation. While CO poisoning is indeed responsible for severe oxygendepletion, the patient presents without cyanosis (white skinned people become a cherry

red). Treatment includes the provision of high flow oxygen.


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respiratory acidosis. Virtually every extended cardiac arrest causes respiratory acidosis(CO2is not being breathed off effectively with cardiac output from CPR only about25% that of normal output).

Low oxygen values often lead to a shift towards anaerobic energy metabolism with by-products such as lactic and pyruvic acids. This increased acidity (lower pH) in theblood is called metabolic acidosis. Similarly, most extended cardiac arrests result inmetabolic acidosis. A return of spontaneous circulation and breathing most often self-corrects both the respiratory and metabolic acidosis (see the section on blood gasanalysis later in this chapter).

Oxygen Transport

Hemoglobin carries about 97% of the bodys oxygen to the tissues. Only about 3% of

oxygen makes its way to the tissues as dissolved oxygen. In order for the oxygen to bepicked up and delivered to the tissues, sufficient quantities of hemoglobin must beavailable.

The normal range of hemoglobin is 120-160 grams of hemoglobin per litre of blood.Each gram can bind with as much as 1.34 ml of oxygen (at 100% saturation). Theamount of oxygen carried by a litre of blood can be calculated as follows:

hemoglobin x 1.34 x O2saturation = oxygen carried / litre of blood

The central parameters that influence blood oxygen content are hemoglobin andoxygen saturation levels. The next three scenarios explore how these parameters as well

as cardiac output can affect the supply of oxygen to the tissues.

Scenario 1:The best case scenario might be a hemoglobin of 150 g and 100% oxygensaturation. A calculator quickly informs us that 1 litre of blood with a hemoglobin of150 g/litre and a saturation of 100% carries about (150 x 1.34 x 1.0) 200 ml of oxygen.With an average cardiac output of 5 litres/minute, about 1 litre (5 x 200 ml) of oxygenis delivered to the body every minute.

Oxygen saturationmeasures the amount of oxygen bound to the hemoglobin. Ahemoglobin that is 100% saturated is carrying a full load of oxygen. Hemoglobin that are

carrying only half the maximum number of oxygen would have an oxygen saturation of

50%. Note that an oxygen saturation of 75% is typical of venous blood returning to the

heart. Each hgb binds with as many as 4 oxygen molecules. So with an O2saturation of

75%, on average only 1 oxygen molecule has been released per hgb leaving most of the

oxygen in reserve.


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of oxygen and glucose to produce adenosine triphosphate (ATP), a molecule that isused in any activity that requires energy. As mentioned several times already, ATPprovides the energy necessary for life.

Because the supply of oxygen and the production of ATP is of primary importance, itshould come as no surprise that several mechanisms ensure that oxygen supply morethan satisfies oxygen (and energy) demand. Respiratory rate, tidal volumes, heart rateand stroke volumes all increase to bring more oxygen to the tissues. At the cellular levelseveral other triggers can cause the hemoglobin to release more oxygen.

The amount of oxygen released to the cells fluctuates with increased energy demand.As aerobic metabolism increases as a response to high demand states (i.e. exercise orfever), CO2- the bi-product of aerobic metabolism - also increases. In response to highenergy demand states, the chemical 2,3 - diphosphoglycerate(2,3-DPG) also increases. Not surprisingly, hemoglobin releases more oxygen to thecells in the presence of elevated amounts of 2,3-DPG, temperature, and CO2(which

causes increased acidity and lower pH). Conversely, low levels of any of these factorsresults in hemoglobin having a higher affinity for oxygen (less oxygen is released).

This all seems rather academic, you might say. How can you apply this information?Oxygen saturation, a topic we will explore further in the next chapter, measures thepercentage of hemoglobin binding sites (four sites/hemoglobin) that are bound tooxygen. When hemoglobins affinity for oxygen decreases, the Pao2is higher for everyoxygen saturation reading i.e. more oxygen is dissociated from the hemoglobin at anyoxygen saturation level.

The good news is that hemoglobin most often has a whole lot more oxygen to share

than is provided during normal resting states. Venous blood has an oxygen saturationof about 75% (3 out of every 4 oxygen binding sites are occupied by oxygen). Duringepisodes of low oxygen content (i.e. anemia, respiratory failure, pneumonia,pulmonary edema) or low oxygen delivery (low cardiac output states such as extremetachycardias or bradycardias and acute heart failure) the body continues to respond bymaking more oxygen available to the tissues.

For healthy individuals at rest, the oxygen supplied is far greater than the oxygen

required. On average, adults require about 250 ml of oxygen each minute to satisfy

metabolic demands (energy demands). In the previous section, we determined thatoxygen content for a healthy adult is about 200 ml per litre. With an average cardiac

output of 5 litres/minute, the body receives about 1000 ml of blood each minute - about

3 times more oxygen than necessary.


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A standard oxyhemoglobin dissociation curve (OHDC) reflects the relationshipbetween hemoglobin oxygen saturation and the partial pressure of arterial oxygen(Pao2). Since oxygen equalizes across the alveolar-capillary membrane quite quickly,the partial pressure of arterial oxygen (Pao2) comes close to equalizing with the partialpressure of alveolar oxygen (PAo2). The ODHC is a graphical relationship between

Pao2and the amount of oxygen carried to the cells (hemoglobins oxygen saturation -see Figure 8.14).

Figure 8.17 Oxyhemoglobin Dissociation Curve

The oxyhemoglobin dissociation curve (OHDC) reflects the amount of oxygen released by thehemoglobin as a function of the arterial oxygen pressures. Certain conditions shift this curveto the left (hgb holds on to more oxygen) or to the right (hgb releases more oxygen). Shifts inthe OHDC left, for example, result in less oxygen released to the tissues for any given PaO2.If you follow the broken line up from a PaO2of 60, oxygen saturations with a shift left wouldincrease from 90% to perhaps 93%. With higher hgb saturation, more oxygen is bound - lessoxygen is released.

During cardiac arrests, ensuing respiratory and metabolic acidosis (high CO2and low

pH) may initially cause the hemoglobin to release more oxygen reserve at the cellularlevel. Many scientists believe that many victims of sudden cardiac arrests (caused by

dysrhythmias) have sufficient stores of oxygen and ATP to help preserve cell function

for at least 4-6 minutes. One caveat: effective cardiac compressions are necessary to

maintain some degree of circulation.

Oxyhemoglobin Dissociation Curve

Left Shift (greater oxygen affinity)

Right Shift (reduced oxygen affinity)

60 80

95

90

T 2,3-DPGH+

pH

T 2,3-DPGH+

CO 2

pH CO 2

Pao2 mm Hg


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The distinct S shape of the OHDC and the tendency of the OHDC to shift left or rightduring certain conditions are important points worth exploring.

The S shaped curve reveals important phenomena. Only a 5% increase in oxygensaturations (from 90% to 95%) occurs with a 33% increase in Pao2(from 60 to 80 mmHg). After a Pao2of 60 mm Hg, increasing inspired oxygen comes with diminishingreturns as the curve plateaus. Breathing high flow oxygen to increase oxygensaturations to more than 95% will not result in substantial increases in blood oxygen

volume (see section on oxygen transport).

The steep slope of the oxyhemoglobin curve reveals precipitous drops in oxygensaturations with Pao2 below 60 mm Hg (or oxygen saturations below 90%). From aclinical perspective, most practitioners consider an oxygen saturation below 90% asignificant finding requiring prompt attention. The steep slope of the oxyhemoglobin

curve supports this concern. Without a rapid response, oxygen saturations couldquickly plummet to levels incompatible with life.

Oxygen saturations for each Pao2 level are not always linear, following the standardcurve. The OHDC can shift to the right or left depending on certain conditions.Increased blood acidity, elevated Pco2, and fever decrease hemoglobins affinity foroxygen with more oxygen released. The OHC shifts right.

Hemoglobin also tends to release more oxygen with increases in the presence of 2,3 -diphosphoglycerate (2,3-DPG). High levels of 2,3-DPG is associated with chronicobstructive pulmonary disease (COPD), anemia, hypoxemia and congestive heart

failure. Each of these can negatively affect blood oxygen volumes. An enhancedproduction of 2,3-DPG apparently serves as an adaptive mechanism, causing the hgbto release more oxygen to the cells.

With a shift of the oxyhemoglobin curve to the right, the hemoglobin is less saturatedat any corresponding Pao2level. Conversely, increased affinity for oxygen is reflectedin a shift to the left for the oxyhemoglobin curve. Here, hemoglobin is more saturatedwith oxygen for every Pao2level resulting in less oxygen availability at the tissues. Thisleft shift occurs with alkalosis, low Co2levels, depleted 2,3-DPG (i.e. bloodtransfusions) and hypothermia.

Tissue oxygenation rarely suffers from just shifts in the OHDC to the left . Morecommonly, tissue oxygenation falls due to abnormally narrow blood vessels andruptured plaques that acutely occlude vessel lumens. An increase in oxygen demandbeyond the limits of oxygen supply for these obstructed vessels can result in ischemiaand infarction. Other conditions that impair tissue oxygenation include shock states,carbon monoxide poisoning, myoglobinemia and sickle cell anemia.


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Flash Quiz 8.3

1. Effective oxygenation requires:

a) gas exchange at the alveolib) transport of oxygen to the cellsc) gas exchange at the cellular leveld) all of the above

2. The term that denotes a low partial pressure of oxygen in the blood is calledhypoxemia.

True or False

3. Gas exchange at the alveoli occurs by:

a) osmosisb) diffusionc) filtrationd) all of the above

4. The main parameters that affect the supply of oxygen to the tissues are:

a) oxygen saturations, cardiac output and fever

b) cardiac output, age and respiratory ratec) hemoglobin, respiratory rate and cardiac outputd) hemoglobin, oxygen saturations and cardiac output

5. An oxygen saturation of 95% or more guarantees sufficient blood oxygen content.

True or False

6. A person who suffers an extended cardiac arrest usually develops (respiratoryacidosis, metabolic acidosis, both respiratory and metabolic acidosis). Upon a return tospontaneous circulation, acidosis is usually corrected within (minutes, days) with

adequate (ventilation, sedation, buffer administration).

7. A person with carbon monoxide poisoning:

a) may be suffocating with oxygen saturation values of 98-100%b) has cyanosis and shortness of breathc) can be cherry red in colourd) a and c

Answers: 1.d) 2.True 3.b) 4.d) 5.False 6.both respiratory and metabolic acidosis, minutes, ventilation 7.d)


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Summary 183

8. Hemoglobin carries about (3%, 60%, 97%) of the oxygen supplied to the body. A shift(right, left) in the oxyhemoglobin dissociation curve occurs when the hemoglobinsaffinity for oxygen decreases (more oxygen is released).

9. The oxyhemoglobin dissociation curve follows an S curve. The steep slope of thecurve signifies the precipitous drop in oxygen content for oxygen saturations below90%.

True or False

10. Hemoglobin releases less oxygen with the following conditions (circle all that arecorrect):

a) alkalosis

b) low CO2levelsc) high 2,3 DPG levelsd) hypothermia

Summary

The structure and function of the respiratory system was explored in this chapter. Thefocus may have sided with how oxygen makes its way to the cells but the effects ofcarbon dioxide are also worth considering. Further discussion on the impact of carbondioxide is provided in the next chapter.

The anatomy of the upper airways efficiently warm, filter and moisturize incoming air.The upper airways account for about 40% of the total airway resistance. Structures suchas the larynx and the cricothyroid cartilage are particularly important duringrespiratory procedures such as endotracheal intubation.

From the trachea, 23 successive branches through each lung takes air flow to theterminal respiratory unit, a respiratory bronchiole and an alveolus. The branches abovethis terminus facilitate air movement but do not engage in gas exchange with the bloodstream. Approximately 300 million alveoli provide ample surface area (about 80 m2) toenable gas exchange with 280 billion pulmonary capillaries. Most of the alveoli (80%)are completely enveloped by pulmonary capillaries.

Oxygen diffuses from the alveoli through to the pulmonary capillaries to increase thePO2from 40 mm Hg to 80-106 mm Hg. Carbon dioxide exits the pulmonarycapillaries to be breathed out into the atmosphere. Oxygen quickly binds to

Answers: 8.97%, right 9.True10.a,b,d


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hemoglobin within red blood cells to be carried to the cells of the body. Only about 3%of the blood oxygen content is freely dissociated. Oxygen content is primarily afunction of hemoglobin levels and oxygen saturation of hemoglobin.

At the cellular level, oxygen is released to migrate freely to the mitochondria whereaerobic metabolism occurs. The amount of oxygen released by the hemoglobin isdirectly related to blood acidity, increased temperature and levels of CO2or2,3-DPG. Hemoglobins reduced oxygen affinity is represented by a shift of theoxyhemoglobin dissociation curve to the right.

Normally, the work of breathing requires only about 2% of cardiac output. Breathingbecomes more arduous with increases in airway resistance and reduced lungcompliance. Reduced elastic recoil, such as occurs to the alveolar walls fromemphysema, leads to airway collapse with rapid or forced expiration. The effort to re-

expand collapsed airways increases the work of inspiration.

Chapter Quiz

1. We breathe to create energy.

True or False

2. The lungs accomplish more than gas exchange. The lungs also:

a) filter the blood of embolib) have an endocrine function,c) clear toxins from the bodyd) all of the above

3. Anaerobic metabolism (with, without) oxygen yields (2, 10, 20, 36) ATP.

4. The many functions of the upper airways include (circle all that are correct):

a) filter air of particulatesb) humidify airc) temperature regulation of air (i.e. warm air)d) allow the ingestion of food and fluidse) aid digestionf) verbal communicationg) safety and security via the sense of taste and smellh) prevent aspiration during eating and during submersion

Answers: 1.True 2.d) 3.without, 2 4.a-h


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Chapter Quiz 185

5. The role of surfactant is to (increase, decrease) surface tension. This in turn(increases, decreases) elastic recoil of the alveoli.

6. A 68 year old man with end-stage chronic obstructive pulmonary disease (COPD) isexperiencing shortness of breath and cardiac ischemia. He is admitted to the ER withan oxygen saturation of 84%. The goal of oxygen therapy for this patient is to deliversufficient oxygen to maintain their oxygen saturation levels at:

a) greater than 95% to aid both the shortness of breath and the cardiacischemiab) 90-92% to help both shortness of breath and cardiac ischemia whilepreventing respiratory depressionc) 86-89% to help both shortness of breath and cardiac ischemia whilepreventing respiratory depression

d) do not provide supplemental oxygen because of the risk of reducingrespiratory drive that can occur with higher oxygen levels

7. Positive pressure ventilation can (increase, decrease) preload to the left side of theheart.

8. Upper airway resistance accounts for about 25-40% of total airway resistance.

True or False

9. If the radius of the bronchioles is reduced by 1/2, bronchiolar airway resistance

increases by:

a) 50%b)200%c) 400%d)1600%

10. For those with emphysema, reduced elastic recoil together with forced expirationcan result in collapsed airways and significantly increased breathing workload.

True or False

11. The drive to breathe is normally linked primarily to blood (O2, CO2) levels.Increases in (O2, CO2) of only 1 mm Hg above a normal mean of (40, 80) mm Hg tendsto increase minute ventilatory volumes by 2-3 litres.

12. The terms respiration and ventilation are interchangeable.

True or False

Answers: 5. decrease, increases 6.b) 7.decrease 8.True 9.d) 10.True 11.CO2, CO2, 40 12.False


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13. The Hering-Breuer reflex is:.

a) a response to increased lung volumes with a reduced respiratory rate

b) also known as the diving reflex associated with the closure of theepiglottis during submersionc) the slowing of heart rate that can occur with the immersion of onesface in ice cold waterd) triggered by receptors in the tendons and joints producing anincreased breathing rate beyond what is physiologically necessary

14. The work of breathing becomes more arduous with increased:

a) inspired volumeb) airway and tissue resistance

c) elastic recoil and lung complianced) a and be) all of the above

15. Effective tissue oxygenation depends on sufficient:

a) cardiac outputb) oxygen saturationc) hemoglobin levelsd) all of the above

16. Does an arterial blood gas value for partial pressure of oxygen (Pao2) provide a goodindication of arterial oxygen content?

Yes or No

17. Which of the following conditions will dramatically impair oxygen transport?

a) slow breathing ratesb) low cardiac output statesc) anemiad) b and c only

e) all of the above

18. At the alveolar level, air velocity is virtually static with the process of diffusion theprimary mobility agent.

True or False

Answers: 13.a) 14.d) 15.d) 16.No 17.d) 18. True


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Chapter Quiz 187

19. About 20% of the alveolar surface (as a whole) is not in contact with pulmonarycapillaries. This non-perfused area is known as:

a) shuntingb) anatomical dead spacec) physiological dead spaced) there is no term for this phenomenon

20. Each day we breathe volumes equivalent to that of a swimming pool and transfergases across a barrier the size of a tennis court.

True or False

21. A V/Q ratio evaluates:

a) blood oxygen contentb) minute ventilation volumec) efficiency of ventilation as a function of PaCO2levelsd) adequacy of ventilation as a function of pulmonary perfusion

22. A V/Q ratio increases with which of the following conditions? (Circle all that apply)

a) emphysemab) pneumoniac) atelectasis

d) low cardiac output statese) low minute ventilation volumef) pulmonary embolusg) tension pneumothorax

23. Red blood cells change their shape to fit through the pulmonary capillaries.

True or False

24. What blood values are typical of the pulmonary arteries for a healthy person at rest?(Circle all that apply)

a) oxygen saturations of 75%b) oxygen saturations of 98%c) PO2of 40 mm Hgd) PO2of 80 mm Hgd) PCO2of 80 mm Hge) PCO2of 45 mm Hg

Answers: 19.c) 20.True 21.d) 22.f 23.True 24.a), c), e)


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25. With an atmospheric pressure of 760 mm Hg at sea level, the inspired partialpressure of oxygen (PO2) of room air is approximately (304, 180, 160, 137, 80) mm Hg.Various face masks that provide approximately 40% inspired oxygen result in an

inspired PO2of (304, 180, 160, 137, 80) mm Hg.

26. Inspired air is soon moisturized in the large upper airways. This humidified air:

a) reduces the PO2furtherb) helps keep mucous produced in the airways loosec) helps to reduce elastic recoild) none of the above

27. Gas exchange is normally completed at the alveoli in about (1/4, 1/2, 3/4, 1) second.This compares favorably to the (1/4, 1/2, 3/4, 1) second that a red blood cell circulates

about the alveoli.

28. Respiratory failure is commonly diagnosed as:

a) PaCO2 > 60 mm Hgb) PaCO2 < 30 mm Hgc) PO2 < 50 mm Hgd) none of the above

29. Carbon monoxide poisoning may not be immediately recognizable. Oxygensaturations are normally (high, low) while nail bed colour is (pink, blue). This can be a

respiratory emergency, nevertheless. The hemoglobins high affinity for carbonmonoxide, (10, 100, 200, 400) times that of oxygen, causes significant deterioration in(alveolar gas exchange, oxygen transport).

30. Blood oxygen content is largely determined by:

a) dissociated oxygen valuesb) hemoglobin levelsc) oxygen saturationd) cardiac outpute) d only

g) b and c onlyf) all of the above

31. A pulseless patient quickly develops both respiratory and metabolic acidosis.

True or False

Answers: 25.160, 304 26. a) 27.1/4, 3/4 28.a) 29.high, pink, 200, oxygen transport 30. g) 31.True


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Chapter Quiz 189

32. Each gram of hemoglobin when fully bound with oxygen can carry about1.34 ml of oxygen. The oxygen content (oxygen volume per litre of blood) for a personwith a hemoglobin of 160 g/litre and an oxygen saturation of 90% is:

a) 214 ml of oxygen per lire of bloodb) 193 ml of oxygen per lire of bloodc) 162 ml of oxygen per lire of bloodd) 141 ml of oxygen per lire of blood

33. An average adult requires about 250 ml of oxygen per minute to sustain life.

True or False

34. Effective oxygen delivery is dependent on the following factors:

a) cardiac outputb) hemoglobin concentrationc) oxygen saturationsd) all of the above

35. A standard oxyhemoglobin dissociation curve depicts the relationship betweenoxygen saturations and oxygen actually delivered to the tissue.

True or False

36. The oxyhemoglobin dissociation curve provides the following importantobservations:

a) incremental increases in oxygen saturations above 90% does notresult in significant increases in available oxygen at the tissuesb) there is not much value in providing supplemental oxygen for thosewith oxygen saturations over 95%c) oxygen saturations decrements below 90% result in plummetingoxygen availability at the tissuesd) all of the above

37. Many experts believe that for those who experience a sudden cardiac death(i.e. due to ventricular fibrillation), oxygen reserves are sufficient to sustain life for thefirst 4-6 minutes in the presence of effective chest compressions.

True or False

Answers: 32.b) 33.True 34.d) 35.False 36.d) 37.True


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38. Circle all parameters that result in more oxygen released to the tissues.

a) low pH

b) high pHc) high PCO2d) hypothermiae) low body temperaturef) increased 2,3-DPG levels

39. More oxygen is released to the tissues for every oxygen saturation when theoxyhemoglobin dissociation curve shifts to the (right, left).

40. On average, there is about (1, 10, 100, 1000) pulmonary capillaries for everyalveolus.

Suggested Readings and Resources

Ball, Dr. Wilmot. (1996). Interactive Respiratory Physiology. John Hopkins School ofMedicine. Found at http://oac.med.jhmi.edu/res_phys/

Levitzky, Michael G. (2003). Pulmonary Physiology. 6th ed. New York: McGraw-Hill

Lingappa, Vishwanath R. (2000). Physiological Medicine. New York: McGraw-Hill

Pulmonary Critical Care Medicine Tutorials. (2003) CCM Tutorials.com. Found athttp://www.ccmtutorials.com/rs/oxygen/index.htm

Whats Next?

This chapter covered pulmonary anatomy, the mechanics of breathing, gas exchange,oxygen transport, and the oxyhemoglobin dissociation curve: a lot to digest.

Chapter 9 builds on this ground work, providing a closer look at three respiratorytechnologies that are commonly used during the cardiac periarrest period: pulseoximetry, end-tidal carbon dioxide monitoring and blood gas analysis. The basicswould not be complete without at least a brief look at these useful respiratoryassessment tools.

@

respiratory basics

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